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The purpose of this study is to evaluate the change of mucosal immunity in gastric diseases. A quantative analysis of IgA and secretory component(SC) in gastric diseases by immunohistochemical method was performed in 110 specimens. The results are as follows: 1) In normal gastric mucosa, all of 10 cases revealed a negative reaction to antihuman SC but 4 cases were positive for IgA. 2) In chronic superficial gastritis and chronic atrophic gastritis with intestinal metaplasia, the metaplastic cells except for the goblet cells were positive for both IgA and SC. 3) The dysplastic cells were also positive for both IgA and SC, and the regenerating cells in ulcer as well. 4) All of the well differentiated or moderately well differentiated adenocarcinomas showed positive reactions to antihuman IgA and antihuman SC, and the intensity appeared to be stronger in the former. However, among 10 cases of poorly differentiated adenocarcinoma SC was not demonstrated in 5 cases, and no IgA was present in one case. In 10 cases of signet ring cell carcinoma, 6 cases revealed a negative reaction to antihuman IgA and 6 cases to antihuman SC. The above results suggest that the secretory immunity is not essential in normal gastric mucosa. The intestinal metaplasia in chronic gastritis is considered as an adaptive response to chronic inflammation. The degree of differentiation in adenocarcinoma may be related to the mucosal immunity.
Adenocarcinoma

A rate com;lication of hysterectomy is complete prolapse and inversion of vagina. This can occur whether the hysterectomy was abdominal or vaginal and cystocele and/or enterocele is often associated with this condition. Traditionally, prolapse has been treated by surgery, the types of operation for prolapse are generally but not always, carried out through the vaginal rather than through the abdominal surgical route. We experienced five cases who had repair of posthysterectomy vaginal vault prolapse by transabdominal sacral colpopexy and report with brief review of literatures.
Cystocele ; Hernia ; Hysterectomy* ; Pelvic Organ Prolapse* ; Prolapse ; Vagina

No abstract available.

The aim of this study was to clarify the role of Kupffer cells in the mechanism of endotoxin-induced liver injury. The study on fine structure of Kupffer cells was performed after the injection of endotoxin. The endotoxin(Escherichia soli lipopolysaccharide 026: B6, 1.5mg/100 g of body weight) was intraperitoneally injected in Sprague-Dewley rats. Animals were sacrificed at 1/4, 1/2, 1, 2, 4, 8, 16, 24, 72 and 120 hours after the injection of endotoxin. Livers were extirpated and processed to be examined by light and electron microscopy. The results obtained were summerized as follows: Early changes observed in liver after endotoxin injection included the increased number and hypertrophy of Kupffer cells, infiltration of neutrophils and presence of fibrin thrombi within the sinusoids. The coritinuous increase of the Kupffer cells in number with hypertrophy, congestion and infiltration of inflammatory cells within the sinusoids were observed. Hepatocytes showed* fatty change and occasional necrosis. At 72 hours the congestion decreased. At 120 hours the number of Kupffer cells was increased, but the morphology of Kupffer cells became similar to that of the control group. The numbers and sizes of primary and secondary lysosomes and amount of euchromatin of Kupffer cells increased. Swellings and increase in number of mitochondria, Golgi complex, smooth endoplasmic reticulum, rough endoplasmic reticulum were evident. Microthrombi were present within the sinusoids. The swelling of rough endoplasmic reticulum and mitochondria, decrease of glycogen particles, fatty change, hypoxic vacuoles, pyknotic nuclei and occasional necrosis were observed in hepatocytes. At 72 hours the number of secondary lysosomes in Kupffer cells decreased. At 120 hours the morphology of Kupffer cells became similar to that of the control group. According to these results, it was postulated that the endotoxin was initially taken up by pinocytosis into Kupffer cells and degraded in secondary lysosomes of activated Kupffer cells. Kupffer cells may play an important role in the defense mechanism of liver during endotoxemia. The dysfunction of Kupffer cells and ischemia by sinusoidal microthrombi may cause liver injury.
Animals ; Endoplasmic Reticulum, Rough ; Endoplasmic Reticulum, Smooth ; Endotoxemia ; Estrogens, Conjugated (USP) ; Euchromatin ; Fibrin ; Glycogen ; Golgi Apparatus ; Hepatocytes ; Hypertrophy ; Ischemia ; Kinetics* ; Kupffer Cells* ; Liver ; Lysosomes ; Microscopy, Electron ; Mitochondria ; Necrosis ; Neutrophils ; Pinocytosis ; Rats* ; Vacuoles